The invention is related to the field of radiofrequency (RF) ablation, and in particular to using Fourier analysis of intracardiac electrograms to assess whether their spectral power distributions could be used to predict ablation sites most likely to result in ventricular tachycardia (VT) termination or termination of other reentrant tachycardia circuits, such as atrioventricular nodal reentrant tachycardia (AVNRT), paroxysmal junctional reciprocating tachycardia (PJRT), or atrioventricular reentrant tachycardias (AVRT) with midseptal accessory pathways, in which the rapidly and slowly conducting limbs of the reentrant circuit lie in close physical proximity to one another.
Ventricular tachycardia (VT), a potentially lethal cardiac arrhythmia, can arise from several different mechanisms. Idiopathic VT is believed to arise from enhanced automaticity, and can often occur in the absence of any apparent structural heart disease. More commonly, VT results from reentry phenomena in association with a narrow isthmus of abnormally conducting tissue that traverses a scar (or scar border) caused by myocardial infarction or other injury. Following such injury, one or more isthmi of abnormally conducting tissue 2 can be located between islands of unexcitable scar tissue 4, or adjacent to some other functionally unexcitable boundary such as a valve annulus, as shown in FIG. 1. Such an isthmus 2 is referred to as the “protected isthmus,” or slow conduction zone, and is critical to the formation of a tachycardia circuit that can support sustained reentry. Rapid conduction zone 6 is associated with normal myocardium and the rapid and slow conduction zones are clearly illustrated using depolarizing wavefronts 8. This substrate can give rise to monomorphic ventricular tachycardia, as judged by both surface and intracardiac electrograms. Thus, monomorphic reentrant ventricular tachycardias (VT) can theoretically occur even if one protected isthmus forms in a scar-related re-entry circuit.
While the current standard of care for the management of most ischemic or scar-related VT is the implantable cardioverting defibrillator (ICD), a significant number of patients with frequent or incessant VT undergo radiofrequency (RF) ablation (or ablation using another lesion generating energy such as cryoablation) of their scar-related substrate. This is usually performed to minimize the number of ICD therapies received by patients who have frequent arrhythmia recurrences despite treatment with medication. Greater than 75% of patients referred for palliative ablation of arrhythmias will have fewer VT recurrences. Less commonly, RF ablation of scar-related VT is performed as first-line therapy for patients with relatively normal LV systolic function and a single known VT substrate.
Recently, there has been renewed interest in VT ablation to prevent or minimize the likelihood of appropriate defibrillator therapies in order to improve patient morbidity and mortality. Catheter ablation of VT may assume an even greater relevance in light of recent studies that demonstrate increased mortality in patients with congestive heart failure that receive frequent shocks from an implanted defibrillator for primary prevention of sudden arrhythmic death.
Several methods are available to identify the location of the VT circuit during ablation procedures. The ability to demonstrate concealed entrainment (with a paced morphology identical to the VT) from a site can be used to determine whether the ablation catheter tip is in direct contact with tissue that contributes to a VT circuit. Commercially available manual and remote three dimensional electroanatomical mapping systems can also be used to create voltage, substrate, and activation sequence maps of the VT circuit. Electrically Unexcitable Scar (EUS) mapping (mapping of pacing thresholds), the presence of late potentials, and electroanatomical mapping can all be used to localize the protected isthmus.
Within the VT circuit, it is important to identify the protected isthmus (slow conduction zone) as the target for the delivery of RF or other ablative energy such as cryoablation or ultrasound ablation lesions. If lesions are not applied at locations within the isthmus (i.e. if they do not connect the unexcitable tissue that bounds the isthmus), then the lesion is likely to only extend the region of scar into otherwise healthy myocardium, and will fail to close the VT circuit. This is probably important in the patient population undergoing scar-related VT ablation procedures, as their ventricular systolic function is often already significantly impaired.
This technique same could be employed to identify the slow conduction zone, or slow limb, of other reentrant tachycardia circuits in which the rapidly and slowly conducting limbs of the reentrant circuit lie in close physical proximity to one another, such as atrioventricular nodal reentrant tachycardia, paroxysmal junctional reciprocating tachycardia, or atrioventricular reentrant tachycardias with midseptal accessory pathways.